AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 251: R591-R597, 1986;
0363-6119/86 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Krueger, J. M.
Right arrow Articles by Davenne, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krueger, J. M.
Right arrow Articles by Davenne, D.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 3 591-R597, Copyright © 1986 by American Physiological Society

ARTICLES

Enhancement of slow-wave sleep by endotoxin and lipid A

J. M. Krueger, S. Kubillus, S. Shoham and D. Davenne

Some muramyl peptides derived from bacterial peptidoglycan enhance slow-wave sleep (SWS). The purpose of this study was to test whether another cell wall component, lipopolysaccharide (LPS), and its lipid A moiety also have an effect on sleep. When injected intravenously, both LPS and lipid A enhanced the duration of SWS, increased electroencephalogram delta-wave amplitudes, suppressed rapid eye movement (REM) sleep, and induced biphasic fevers. The effects of intravenously administered lipid A and LPS on SWS were present primarily during the first 3 h postinjection. Intraventricular lipid A administration enhanced SWS, did not suppress REM, and induced a monophasic fever; the SWS effect had a 3-h latency, whereas temperature started to rise during the second hour. Regardless of the route of administration, within the dose range used here, sleep was normal by the following criteria: sleep was episodic, animals could be easily aroused, and brain temperature, although elevated to "febrile" levels, continued to fluctuate during sleep-state transitions indistinguishably from control conditions. We conclude that LPS and lipid A are capable of modulating sleep.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
K. A. Jhaveri, V. Ramkumar, R. A. Trammell, and L. A. Toth
Spontaneous, homeostatic, and inflammation-induced sleep in NF-{kappa}B p50 knockout mice
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2006; 291(5): R1516 - R1526.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online